MyAccess Sign In

About MyAccess

If your institution subscribes to this resource, and you don't have a MyAccess Profile, please contact your library's reference desk for information on how to gain access to this resource from off-campus.

KEY POINTS

Clinically, acute PE can be classified as either massive or submassive. Thrombolytic therapy is the recommended treatment for patients with acute massive PE who are hemodynamically unstable and do not have a high bleeding risk.

In patients with submassive PE, the use of thrombolytic therapy remains controversial.

Risk stratification with echocardiography may assist when deciding to use thrombolytic therapy for hemodynamically stable patients with submassive PE and evidence of right ventricular (RV) dysfunction.

Echocardiographic findings in patients with acute PE include RV hypokinesis and dilatation, interventricular septal flattening and paradoxical motion toward the left ventricle, tricuspid regurgitation, pulmonary hypertension and loss of inspiratory collapse of the inferior vena cava.

The hemodynamic status of the patient with acute PE is the most significant predictor of mortality in the short term.

Among patients with submassive PE being treated with unfractionated heparin, the administration of tenecteplase reduced the composite endpoint of all-cause mortality or hemodynamic decompensation at 7 days when compared to placebo but was associated with an increased rate of bleeding.

INTRODUCTION

Acute pulmonary embolism (PE) remains the most frequent and potentially fatal venous thromboembolic event. It is estimated that 100,000 to 180,000 deaths occur annually in the United States from acute PE. The outcome of acute PE depends on both the severity of pulmonary arterial obstruction and the presence and severity of preexisting cardiopulmonary disease in the patient. Acute PE can be classified as massive or submassive. Massive PE accounts for 5% of patients with acute PE and is associated with hypotension (defined as systolic blood pressure [SBP] less than 90 mm Hg or a decrease in SBP of 40 mm Hg or more from baseline) and frequently results in acute right ventricular (RV) failure. Submassive PE accounts for approximately 20% to 25% of patients with acute PE and is associated with normotension and evidence of RV dysfunction including RV enlargement documented by transthoracic echocardiography or computed tomographic (CT) pulmonary angiography and elevated biomarkers of myocardial injury (troponins I or T- and B-type natriuretic peptide [BNP]).1,2,3

The recent guidelines from the American College of Chest Physicians and American Heart Association recommend treatment with thrombolytic agents for patients with acute massive PE who present with persistent hypotension and do not have a high bleeding risk.4,5 Several studies have demonstrated that thrombolytic therapy offers angiographic and hemodynamic benefits compared with standard heparin anticoagulation for patients with acute PE.4,5 The most studied thrombolytic agents for the treatment of PE are recombinant-tissue-type plasminogen activator (TPA, alteplase), streptokinase, and recombinant human urokinase. Other agents include tenecteplase, and reteplase. Absolute contraindications include any prior intracranial hemorrhage, known structural intracranial cerebrovascular disease (eg, arteriovenous malformation), known malignant intracranial neoplasm, ischemic stroke within 3 months, suspected aortic dissection, active bleeding or bleeding diathesis, ...